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First Trimester Nausea: The Maladaptive Phenomenon

Carlotta Ceccarelli

24th May 2023

Experiencing nausea during the first trimester of pregnancy has coined the term ‘morning sickness’ to describe gestational nausea and vomiting. This colloquial term is a total misnomer, considering this particular sensation of needing to throw up does not just occur in the ‘morning’ and is definitely no disease connoted by ‘sickness’. For the sake of accuracy, nausea and/or vomiting during pregnancy will be referred to as NVP. The earliest phase of pregnancy, known as the first trimester, summons a series of changes in the mother which can include novel food aversions. Conditioned taste aversions are common after associating foods with being ill such as having food poisoning, but they are induced by adverse past experiences and are not usually time restrained which is untrue for pregnancies. NVP is not caused by the demands of pregnancy, it doesn’t negatively affect the body’s vital functions nor is it an indicator of bad health; it can’t constitute the definition of a disease. In fact, women who experienced NVP to a greater extent during pregnancy miscarried less often and showed more positive pregnancy outcomes than those who experienced lighter ‘symptoms’ (Sherman and Flaxman, 2002). Despite how maladaptive it is for mother and foetus to risk a decrease in calories that are responsible for foetal growth, NVP correlates with improved foetal survival and infant health (Mckerracher, Collard and Henrich, 2015). Evolutionary hypotheses can explain how such a burdensome phenomenon has not yet been eliminated by natural selection; perhaps NVP is a display of optimal defence system operation, rather than a bodily malfunction.


Predictions of the very first NVP selective pressures date to a time period between 1.8 million and half a million years ago, when humans survived as hunter-gatherers and food foragers (Cardwell, 2012). Early hominids struggled to safely stash food that was leftover after feeding, especially as they became more capable of hunting larger animals. Meat-borne infections were still prevalent as a consequence of eating dangerous microorganisms and toxins present in raw meat. Toxoplasmosis, a disease caused by undercooked meat, is linked with birth abnormalities, spontaneous miscarriages and neonatal conditions (Sherman and Flaxman, 2002). When Homo erectus began cooking their food, it was more calorically favourable and less likely to contain harmful pathogens; however, it did not eliminate all toxin potentiality. Cooking meat introduced additional hazards when using various utensils such as sticks, leaves and earthenware (Cardwell, 2012). Since meat was a prominent component in ancestral human diets, there was a rise in selective pressure on humans to develop the nauseating feeling of disgust. The adaptation of rejecting oral incorporation of certain foods was advantageously selected against those who did not have the acquired guard against disease. Similarly, this can be applied to pregnant women, with the function of protecting the foetus from suffering the result of toxoplasmosis.


The most evidence supports the Maternal-Embryo Protection Hypothesis (MEPH), which describes NVP as a protection mechanism for mother and foetus against pathogenic substances in meat products and toxins in strong-tasting plants. Humans reproduce sexually, meaning that half of the foetus’ genome contains its fathers’ cells, which are biologically foreign to the mother. In order for the foetus to not be attacked, mothers need to temporarily suppress their immune systems so that they can tolerate the foetus’ tissues and not target them as ‘non-self’ (Mckerracher, Collard and Henrich, 2015). Simultaneously, the foetus is in the biological process of organogenesis. This is the most vulnerable stage of foetus development, where complete organs emerge, and the time window is subject to the most wide-ranging effects if disrupted by food-borne illnesses (Fessler, Eng and Navarrete, 2005). Both factors explain why NVP is usually limited to the first 12 weeks of gestation. Consequently, women most commonly have taste aversions towards meat, eggs, vegetables and caffeinated beverages. These foodtypes were found to be most likely to contain food-derived teratogens and abortifacients, agents that can induce foetal abnormalities or abortion if ingested. Diet directly correlates with the effects of NVP, confirmed by the fact that few societies lack the typical nauseous indicators of this adaptation. Maize and rice tend to be the staple foods in these groups; the plants effuse significantly fewer secondary compounds and distinct aromatic chemicals designed to deter the crops’ biotic enemies (Sherman and Flaxman, 2002). They are also rich in the vitamin folic acid, a primary component of prenatals for its preventive measures against foetus neural tube defects. They are commonly dehusked and dried during preparation which increases pathogenic microorganism resistance (Profet, 1992). While this diet suppresses NVP without any negative consequences, Fessler (2002) demonstrates that most women have a compensatory mechanism in the form of ‘craving’ alternative protein sources. The appeal of dairy is said to help atone for the costly results of meat aversions, which leads to the questions, what about the societies that have slender substitutions to meat and do not depend on dairy like the indigenous Inuit? How would Sherman and Flaxman (2002) explain a newly pregnant woman in an arctic winter, wouldn’t raw meat be a good source of vitamin C (Fessler, 2002)? A substantial limitation of Sherman and Flaxman (2002) was the study subjects primarily come from large-scale societies, this indicates that the results could be favoured by the fact that all society ranges were affiliated as one. In light of this, looking at Mckerracher, Collard and Henrich (2015) provided a smaller-scale dataset based on Yasawa Island, Fiji. Despite having different local food production and health systems, NVP prevails cross-culturally as 67% of women within their first two trimesters reported experiencing ‘Kune ca’, the western Fijian equivalent of ‘morning sickness’. Not only were comparable meat and strong-smelling vegetable sources equally aversive, but so were the scents of their romantic partners. Phenomenally, the aversion of their husbands shows a correspondence with MEPH; pathogens can be shared in an additional way they aren’t with other foreign sources- sexual transmission. This exposure is equally unfavourable for a pregnant woman with a depressed cell-mediated immune response carrying a foetus during organogenesis (Mckerracher, Collard and Henrich, 2015). Regardless of the smaller-scale demographic, the food categories in question were compared to American disease control standards. Foodstuffs across cultures are assembled and consumed completely differently, meaning the pathogenicity of Fijian animal foods could be entirely over/underestimated. Gathering data on an island that lacks comprehensive food-borne contaminant information seems counterintuitive, proving the deficiency of all society ranges being combined as one.


The Compensatory Placental Growth (CPGH) and By-product (BPH) hypotheses represent the idea that mother and foetus have different genetic investments, where a shortage of maternal resources can cause conflict. The CPGH states that embryos exploit the source of energy required for placental development, by reducing maternal appetite in the form of NVP, counteracting their ‘energetic’ incompatibilities. Therefore, women are adapted to avoid maternal weight gain by being put off nutrient-dense foods. However, studies conclude that food macronutrient density is not the reason for developed food aversions nor did it have a relationship with NVP (Mckerracher, Collard and Henrich, 2015; Pepper and Craig Roberts, 2006). Naturally, this theory would suggest lightweight women with a more narrow caloric reserve would have elevated rates of NVP, as maternal-foetal conflict would be more pronounced. In contrast, Vikanes et al. (2010) show heavier mothers experience NVP most frequently. The BPH claims to have the same outcome, except it holds that hormonal signals are responsible for the effects of NVP. This means that pregnant females experience NVP no matter the external trigger, which abnormally does not apply to all mammals, regardless of the fact that mother-offspring conflict would be expected to occur in all placentalia (Flaxman and Sherman, 2008). Not only do these alternative hypotheses fall short of explaining food aversions, but they also do not correspond to the ‘energetic’ demands of the foetus according to gestation. They fail to interpret why NVP tapers off only in the early phases of pregnancy, as the third trimester arguably amounts to a high foetal energetic demand.


MEPH is the most well-founded hypothesis that addresses the historical persistence of NVP as an adaptation. It provides logical explanations for the preventative measures today such as avoiding mould-ripened cheeses, cold cured meats and raw fish in sushi during pregnancies. NVP should be labelled for the adaptation that it is, terms such as ‘sickness’ and ‘symptoms’ that insinuate pathology are a reason its associations fall short. We now live in a world where modern medicine, chemical preservatives and technology such as refrigeration exists; the difficulties we once faced as hunting hominids are quite literally out of date. This is why it is believed that through evolutionary time, NVP will become increasingly maladaptive, with nature eventually selecting the most well-nourished mother who does not experience the distress and loss of calories that NVP can induce. With technology advancing to the point of potentially replacing the protective mechanism, it appears the costs of NVP in pregnancy will eventually far outweigh the benefits. Or perhaps the inevitable introduction of new toxins of the future will feed NVP’s perpetual cycle of adjusting environmentally induced selections.





Bibliography:

Cardwell, M.S. (2012) ‘Pregnancy Sickness: A Biopsychological Perspective’, Obstetrical & Gynecological Survey, 67(10), pp. 645–652. Available at: https:// doi.org/10.1097/OGX.0b013e31826ff6c5.

Fessler, D.M.T. (2002) ‘Reproductive Immunosuppression and Diet: An Evolutionary Perspective on Pregnancy Sickness and Meat Consumption’, Current Anthropology, 43(1), pp. 19–61. Available at: https://doi.org/10.1086/324128.

Fessler, D.M.T., Eng, S.J. and Navarrete, C.D. (2005) ‘Elevated disgust sensitivity in the first trimester of pregnancy: Evidence supporting the compensatory prophylaxis hypothesis’, Evolution and Human Behavior, 26(4), pp. 344–351. Available at: https:// doi.org/10.1016/j.evolhumbehav.2004.12.001.

Flaxman, S.M. and Sherman, P.W. (2008) ‘Morning Sickness: Adaptive Cause or Nonadaptive Consequence of Embryo Viability?’, The American Naturalist, 172(1), pp. 54–62. Available at: https://doi.org/10.1086/588081.

Mckerracher, L., Collard, M. and Henrich, J. (2015) ‘The expression and adaptive significance of pregnancy-related nausea, vomiting, and aversions on Yasawa Island, Fiji’, Evolution and Human Behavior, 36(2), pp. 95–102. Available at: https://doi.org/ 10.1016/j.evolhumbehav.2014.09.005.

Pepper, G.V. and Craig Roberts, S. (2006) ‘Rates of nausea and vomiting in pregnancy and dietary characteristics across populations’, Proceedings of the Royal Society B: Biological Sciences, 273(1601), pp. 2675–2679. Available at: https:// doi.org/10.1098/rspb.2006.3633.

Profet M. (1992) ‘Pregnancy sickness as adaptation: a deterrent to maternal ingestion of teratogens’. In: Barkow JH, Cosmides L, Tooby J, eds. ‘The Adapted Mind: Evolutionary Psychology and the Generation of Culture’, New York: Oxford University Press, pp.327–365.

Sherman, P.W. and Flaxman, S.M. (2002) ‘Nausea and vomiting of pregnancy in an evolutionary perspective’, American Journal of Obstetrics and Gynecology, 186(5), pp. S190–S197. Available at: https://doi.org/10.1067/mob.2002.122593.

Vikanes, Å. et al. (2010) ‘Maternal Body Composition, Smoking, and Hyperemesis Gravidarum’, Annals of Epidemiology, 20(8), pp. 592–598. Available at: https:// doi.org/10.1016/j.annepidem.2010.05.009.

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